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Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction

Beteiligung von kieferorthopädischer Belastung an der entzündungsvermittelten Destruktion des Parodontiums

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Journal of Orofacial Orthopedics / Fortschritte der Kieferorthopädie Aims and scope Submit manuscript

Abstract

Aim:

Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation.

Materials and Methods:

PDL cells (from six donors) grown on BioFlex® plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05).

Results:

In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals.

Conclusion:

These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation.

Zusammenfassung

Hintergrund und Ziel:

Unsachgemäß durchgeführte kieferorthopädische Zahnbewegungen wie auch okklusale Überbelastungen können eine parodontitisinduzierte Destruktion des Parodontiums verstärken. Die zugrunde liegenden Mechanismen für den destruktionsverstärkenden Effekt der biomechanischen Belastung sind jedoch noch ungeklärt. In dieser In-vitro-Studie sollte untersucht werden, ob biomechanische Kräfte die Reaktion von parodontalen Ligament-(PDL-)Zellen auf Entzündungsreize modulieren.

Material und Methodik:

Auf BioFlex®-Platten kultivierte PDL-Zellen von sechs Patienten wurden mit Interleukin (IL) 1β, das an entzündeten parodontalen Stellen erhöht ist, inkubiert und/oder einer zyklischen Zugbelastung (CTS) niedriger (3%) und hoher (20%) Stärke für 1 und 6 Tage ausgesetzt. Die Synthese von proinflammatorischen Mediatoren (IL1β, IL8, COX2), Wachstumsfaktoren (IGF1, VEGF, TGFβ1), Kollagen Typ 1 (COL1) und osteogenen Proteinen (ALP, RUNX2) wurde mittels Real-Time-PCR und ELISA analysiert. Die Rate der Wundauffüllung wurde mit einem In-vitro-Wundheilungsassay untersucht. Für die statistische Auswertung kamen der Student’s t-Test und ANOVA zur Anwendung (p<0,05).

Ergebnisse:

Im Allgemeinen wurde die IL1β-induzierte Expression der proinflammatorischen Mediatoren durch CTS am Tag 1 signifikant verstärkt und am Tag 6 signifikant gehemmt. CTS hoher Stärke reduzierte signifikant die IGF1-Synthese, führte aber zu einer signifikanten Steigerung von VEGF unter normalen und entzündlichen Bedingungen. CTS hemmte im Allgemeinen auch die IL1β-induzierte Expression von COL1, ALP und RUNX2. Ab dem fünften Tag wurde die geringste Wundheilungsrate in den Kulturen beobachtet, die gleichzeitig entzündlichen und biomechanischen Signalen ausgesetzt waren.

Schlussfolgerung:

Diese Ergebnisse legen nahe, dass kieferorthopädische und okklusale Kräfte zur parodontalen Destruktion durch Herunterregulation extrazellulärer Matrixproteine und osteogener Differenzierungsmarker, jedoch nicht durch Verstärkung der parodontalen Entzündung bei Parodontitispatienten beitragen könnten.

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Authors and Affiliations

  1. Clinical Research Unit 208, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany

    Marjan Nokhbehsaim, Birgit Deschner, Christoph Bourauel, Søren Jepsen, Andreas Jäger &  James Deschner

  2. Department of Periodontology, Operative and Preventive Dentistry Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany

    Marjan Nokhbehsaim, Jochen Winter, Søren Jepsen &  James Deschner

  3. Department of Orthodontics, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany

    Birgit Deschner & Andreas Jäger

  4. Oral Technology, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany

    Susanne Reimann & Christoph Bourauel

  5. Clinical Research Unit 208, Department of Periodontology, Operative and Preventive Dentistry Center of Dento-Maxillo-Facial Medicine University of Bonn, Welschnonnenstraße 17, 53111, Bonn, Germany

    James Deschner

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  1. Marjan Nokhbehsaim
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Correspondence to James Deschner.

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Nokhbehsaim, M., Deschner, B., Winter, J. et al. Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction. J Orofac Orthop 71, 390–402 (2010). https://doi.org/10.1007/s00056-010-1031-7

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  • DOI: https://doi.org/10.1007/s00056-010-1031-7

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